Histological Properties of Placentas in Acute Herpes Simplex Virus Infection Affecting Genitals

Z. Vorontsova, O. D. Zhilyaeva, V. V. Shishkina, S. Zolotareva, T. V. Samoilenko, E. S. Goryushkina, L. N. Antakova
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Abstract

Acute herpes simplex virus infection in pregnant women results in intrauterine infection of the fetus in 45–50% of cases, thus being the cause of septic complications and severe somatic and neurological disorders in the newborn.The aim of the study was to investigate the placentas of new mothers with newly diagnosed herpes simplex virus type 2 infection (HSV-2) using histological and immunochemical methods.Material and methods. This histological study included 10 placentas of new mothers after operative delivery by caesarean section with newly diagnosed HSV-2 infection. The comparison group (control) consisted of 10 placentas of women with a physiological pregnancy. Histological sections of the placenta were stained with hematoxylin and eosin, Giemsa's solution and Picro-Mallory staining. Identification of the pro- and antiinflammatory phenotype of macrophages (CD68, CD163), subpopulations of CD4 and CD8 lymphocytes, TLR4 receptor expression was performed by immunohistochemical method using specific antibodies. Quantification of the cell population and TLR4 receptors was performed morphometrically. The data obtained were statistically analysed using MS Excel (2016) and SPSS Statistics 17.0.Results. Morphological manifestations of acute herpes simplex virus infection were combined inflammatory and compensatory in nature in the third trimester of pregnancy. The histological picture of the fetal part of the placenta demonstrated a decreased number of M2 (antiinflammatory) macrophages and an increased number of M1 (pro-inflammatory) macrophages. The imbalance between CD163+ and CD68+ profiles of placental macrophages with the numerical predominance of the latter evidenced a pronounced cellular immune response; this, in turn, was supported by intense TLR4 immunopositive staining of the fetal part of the placenta. There was perivillous fibrin deposition of varying degrees, villus agglutination, and necrosis of trophoblast cells associated with a relatively small population of CD4+ and CD8+. Villitis of viral etiology was characterized by destructive infiltration of maternal CD8+ T-lymphocytes penetrating the chorionic villi, combined with activated macrophages in the villi of the fetal part of the placenta. Modifications in the proportion of immune cells during HSV-2 infection supported cytotoxic and autoimmune reactions in the placenta in response to HSV-2 introduction.Conclusion. The results obtained evidence the development of a pronounced immunopathological process in the tissues of the fetal part of the placenta, which results in the decreased protective and compensatory properties of the placenta and increases risk of perinatal complications.
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影响生殖器的急性单纯疱疹病毒感染的胎盘组织学特征
孕妇急性单纯疱疹病毒感染导致45-50%的胎儿宫内感染,从而导致新生儿脓毒性并发症和严重的躯体和神经疾病。本研究的目的是用组织学和免疫化学方法研究新诊断为单纯疱疹病毒2型感染(HSV-2)的新妈妈的胎盘。材料和方法。本组织学研究包括10例新诊断为HSV-2感染的剖宫产术后新妈妈的胎盘。对照组为生理妊娠妇女胎盘10个。胎盘组织切片采用苏木精染色、伊红染色、吉氏染色和Picro-Mallory染色。采用特异性抗体免疫组化方法检测巨噬细胞(CD68、CD163)、CD4和CD8淋巴细胞亚群、TLR4受体表达的促炎表型和抗炎表型。定量细胞群和TLR4受体进行形态计量学。采用MS Excel(2016)软件和SPSS Statistics 17.0.Results软件对所得数据进行统计分析。急性单纯疱疹病毒感染在妊娠晚期表现为炎症性和代偿性相结合。胎盘胎儿部分的组织学图显示M2(抗炎)巨噬细胞数量减少,M1(促炎)巨噬细胞数量增加。胎盘巨噬细胞CD163+和CD68+谱的不平衡与后者的数量优势证明了明显的细胞免疫应答;这反过来又得到胎盘胎儿部分TLR4免疫阳性染色的支持。绒毛周围有不同程度的纤维蛋白沉积,绒毛凝集,滋养细胞坏死,CD4+和CD8+细胞相对较少。病毒性绒毛炎的特点是母体CD8+ t淋巴细胞穿透绒毛膜绒毛的破坏性浸润,并结合胎盘胎儿部分绒毛中活化的巨噬细胞。HSV-2感染期间免疫细胞比例的改变支持胎盘对HSV-2引入的细胞毒性和自身免疫反应。结果表明,胎盘胎儿部分的组织发生了明显的免疫病理过程,导致胎盘的保护性和代偿性降低,增加了围产期并发症的风险。
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